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AIM:Hepatic ischemia/reperfusion injury may cause acuteinflammatory,significant organ damage or dysfunction,andremains an important problem for liver transplantation.Our previous in vivo and in vitro studies demonstrated thatYisheng injection(YS),a traditional Chinese medicine,hadprotective effect on ischemia/reperfusion injury.In thisstudy,we examined whether YS had protective effect forhepatic ischemia/reperfusion injury and explored itsprotective mechanism.METHODS:Hepatic warm ischemia/reperfusion wasinduced in mice.YS at different doses(5,10,20 mg/kg)was injected intraperitoneally 24 h and 1 h before ischemiaand a third dose was injected intravenously just beforereperfusion.The hepatocellular injury,oxidative stress,neutrophil recruitment,proinflammatory mediators andadhesion molecules associated with hepatic ischemia/reperfusion injury were assayed by enzyme-linkedimmunosorbent assay(ELISA),immunohistochemical assayand reverse transcription polymerase chain reaction(RT-PCR).RESULTS:Undergoing 90 min of ischemia and 6 h ofreperfusion caused dramatical injuries in mouse livers.Administration of YS at doses of 5,10 and 20 mg/kgeffectively reduced serum levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST)and lactatedehydrogenase(LDH),from 3 670±463 U/L,2 362±323 U/Land 12 752±1 455 U/L in I/R group to 1 172±257 U/L,845±193 U/L and 2 866±427 U/L in YS(20 mg/kg)treatedgroup,respectively(P<0.01).The liver myeloperoxidase(MPO)and malondialdehyde(MDA)contents were decreasedfrom 1.1±0.2(U/mg protein)and 9.1±0.7(nmol/mgprotein)in I/P,group to 0.4±0.1(U/mg protein)and5.5±0.9(nmol/mg protein)in YS(20 mg/kg)treatedgroup,respectively(P<0.01).Moreover,the serum levelsof tumor necrosis factor-alpha(TNF-α)were reduced from55±9.9(pg/mL)in I/R group to 16±4.2(pg/mL)(P<0.01).Furthermore,the over-expressions of TNF-α andintercellular adhesion molecule-1(ICAM-1)were suppressedby YS treatment in a dose-dependent manner.CONCLUSION:YS attenuates hepatic warm ischemia/ reperfusion injury by reducing oxidative stress and suppressingthe over-expression of proinflammatory mediators andadhesion molecules.
AIM:Hepatic ischemia/reperfusion injury may cause acute inflammatory, significant organ damage or dysfunction,andremains an important problem for liver transplantation.Our previous in vivo and in vitro studies showed that Yisheng injection(YS),a traditional Chinese medicine,hadprotective effect on ischemia/ Reperfusion injury.In thisstudy,we examined whether YS had protective effect forhepatic ischemia/exchange injury and explored itsprotective mechanism.METHODS:Hepatic was ischemia/reperfusion was induced in mice.YS at different doses(5,10,20 mg/kg)was injected Intraperitoneally 24 h and 1 h before ischemia and a third dose was intravenously just before rehabilitation.The hepatocellular injury,oxidative stress,neutrophil recruitment,proinflammatory mediators and adhesion lenses associated with hepatic ischemia/reperfusion injury were assayed by enzyme-linked immunophoresorb assay (ELISA),immunohistochemical Assay and reverse transcription polymerase chain reaction (RT-PCR).RESULT S:Undergoing 90 min of ischemia and 6 h of reperfusion caused dramatical injuries in mouse livers.Administration of YS at doses of 5,10 and 20 mg/kgeffectively reduced serum levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST) and lactatedehydrogenase( LDH), from 3 670±463 U/L, 2 362±323 U/Land 12 752±1 455 U/L in I/R group to 1 172±257 U/L, 845±193 U/L and 2 866 ± 427 U/L in YS (20 mg/kg) treatedgroup, respectively (P<0.01). The liver myeloperoxidase (MPO) and malondialdehyde (MDA) contents were decreased from 1.1±0.2 (U/mg protein) and 9.1±0.7 ( Nmol/mgprotein)in I/P,group to 0.4±0.1(U/mg protein)and5.5±0.9(nmol/mg protein)in YS(20 mg/kg)treatedgroup,respectively(P<0.01).Moreover, The serum levels of tumor necrosis factor-alpha(TNF-α)were reduced from55±9.9(pg/mL) in I/R group to 16±4.2(pg/mL)(P<0.01).Furthermore,the over-expressions of TNF-α and intercellular adhesion molecule-1(ICAM-1)were suppressed by YS treatment in a dose-dependent manner.CONCLUSION:YS attenuates hepatic Trk/ reperfusion injury by reducing oxidative stress and suppressingthe over-expression of proinflammatory mediators andadhesion molecules.